CAR-T With Nine Engineered Edits Shrinks Colorectal Tumours

Early clinical results suggest that FT836, an off-the-shelf CAR T-cell therapy derived from induced pluripotent stem cells (iPSCs), may induce tumour regression in heavily pre-treated metastatic colorectal cancer without the need for lymphodepleting conditioning chemotherapy. The engineered cells were also detected within tumour tissue, indicating successful trafficking and persistence in patients with intact immune systems.

By: Gorm Palmgren - Jun. 3, 2026
News

FT836 is designed to target the stress-induced tumour antigens MICA and MICB, which are broadly expressed across many solid tumours. At the ASCO Annual Meeting 2026, Fate Therapeutics reported preliminary Phase 1 data from nine patients treated with FT836 in combination with either cetuximab or trastuzumab. No dose-limiting toxicities, cytokine release syndrome, immune effector cell-associated neurotoxicity syndrome, or graft-versus-host disease were observed.

Among the first efficacy-evaluable patients with KRAS wild-type metastatic colorectal cancer, investigators reported reductions in target lesion size and tumour biomarkers despite extensive prior treatment histories. FT836 was detected in peripheral blood shortly after infusion and later in tumour biopsies, where treatment was associated with remodelling of the tumour immune microenvironment and increased proximity between endogenous CD8-positive T cells and tumour cells.

FT836 is notable for incorporating nine genetic modifications into a single clonal iPSC-derived cell product. Publicly disclosed engineering includes a MICA/B-directed CAR, an alloimmune defence receptor (ADR), CD58 knockout, a high-affinity non-cleavable CD16 receptor (hnCD16), the CXCR2 trafficking receptor, and a TGFβ signal-redirection receptor. Together, these modifications are intended to improve tumour recognition, enhance migration into tumour tissue, support antibody-dependent cellular cytotoxicity, counteract immunosuppressive signalling and reduce immune-mediated rejection. The remaining edits have not been fully disclosed publicly.

Fate Therapeutics describes the manufacturing process as precise multiplex engineering of a parental iPSC line, followed by selection of a single engineered clone for large-scale production. Although the company has not explicitly stated that FT836 was generated using CRISPR, Fate’s broader iPSC platform employs CRISPR-based genome engineering technologies, including licensed MAD7 nuclease systems, making CRISPR-mediated editing the likely method used to introduce the multiple genomic modifications required for FT836.

The study results were reported by Fate Therapeutics in a press release on 1 June 2026.

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